The development of diabetes is said to be associated with two factors, namely, a decrease in insulin secretion and an insulin resistance. Recently, a greater number of Japanese people have become afflicted with diabetes. Since the decrease in insulin secretion mostly is attributable to genetic factors, it is considered that a major cause of the increase in the number of diabetics is not the decrease in insulin secretion but the insulin resistance. Such an insulin resistance reportedly is caused by an increase in fat intake due to westernized dietary habits of Japanese people as well as lack of exercise, obesity and stress. Recent studies have revealed that the mechanism of the occurrence of insulin resistance is ascribable to hypertrophic adipocytes. In other words, hypertrophic adipocytes cause TNF-α and free fatty acid (FFA) to be secreted, thus not only impairing the sugar intake in muscle cells and liver cells but also inhibiting the secretion of adiponectin, which promotes a function of insulin, so that the insulin resistance occurs.
On the other hand, studies of the insulin resistance have shown that the activation of PPARs, which are intranuclear receptors, is effective in relieving the insulin resistance. PPARs are known to have three types, i.e., α, σ and γ, and several subtypes. PPARα is expressed mainly in the liver cells and also in other cells such as myocardial cells and gastrointestinal cells, and associated with fatty acid oxidation, ketogenesis and apolipoprotein generation. Although PPARσ is not considered to have tissue specificity and is expressed throughout the body, it is expressed notably in colon cancer cells. PPARγ can be classified into two subtypes, i.e., type γ1 and type γ2. The type γ1 is expressed in adipose tissues, immune system tissues, the adrenal gland and the small intestine, whereas the type γ2 is expressed specifically to adipocytes and plays an important role in differentiation induction of the adipocytes and fat synthesis.
As described above, PPARs greatly are involved with the relief of insulin resistance. In addition, PPARs are said to be associated with the relief of hyperinsulinism, type II diabetes as well as obesity, hypertension, hyperlipemia and arteriosclerosis. From this viewpoint, studies have been conducted on substances that activate PPARs, and synthetic substance-based PPAR activators such as fibrate compound, thiazolidine derivatives, fatty acids, leukotriene B4, indomethacin, ibuprofen, fenoprofen, and 15-deoxy-Δ-12,14-PGJ2 are known, for example. However, since such synthetic substance-based PPAR activators have a problem of side effects caused by long-term intake, they are not suitable for preventing or relieving diseases such as the insulin resistance by daily intake. Other than the above, natural substances such as curcumin contained in turmeric, monoacylglycerol, which is one kind of fats and oils, catechins contained in tea, etc. have been reported as PPAR activators derived from natural components (see Patent document 1, for example). However, fats and oils have a high calorie content, though they are derived from natural components, and therefore, a problem arises if they are taken continuously. Further, although it is ideal that the natural component-derived PPAR activators be added to foods or the like for daily intake, they are not suitable for the addition to foods or the like because they often have peculiar tastes.
Patent document 1: JP 2002-80362 A